Vascular dementia (VaD) is a mental disorder caused by brain damage due to cerebrovascular disease, and incidence of VaD is rising. To date, there is no known effective cure for VaD, so effort in developing an effective treatment for VaD is of great importance. The differentiation plasticity of BMSCs, in conjunction with its weak immunogenicity, makes manipulated BMSCs an attractive strategy for disease treatment. However, BMSCs often display disabled differentiation, premature aging, and unstable proliferation, reducing their neuroprotective function. These problems may be caused by the lack of telomerase activity in BMSCs. Our results show that NGF-TERT co-transfected BMSCs have a better therapeutic effect than BMSCs lacking NGF and TERT expression, demonstrated by significant improvements in learning and memory in VaD rats. The underlying mechanism might be increased expression of NGF, TrkA and SYN in the hippocampal CA1 area, which has potential implication in advancing therapeutics for VaD.